Citalopram and the KCNE1 D85N variant: a case report on the implications of a genetic modifier

• Published in: European heart journal. Case reports Vol. 2; no. 4; p. yty106
• Main Authors: Marstrand, Peter, Christensen, Alex Hørby, Bartels, Emil Daniel, Theilade, Juliane
• Format: Report
• Language: English
• Published: 01.12.2018
• ISSN: 2514-2119
• DOI: 10.1093/ehjcr/yty106

BACKGROUNDProlongation of the QT interval on the electrocardiogram is clinically important due to the association with an increased risk of sudden cardiac death. A long QT interval may be genetically determined (congenital long QT syndrome) or be drug-induced long QT syndrome e.g. caused by pharmaceutical drugs and electrolyte imbalances. CASE SUMMARYIn this report, we describe the case a 54-year-old woman, who presented with syncope. At presentation, the QTc interval was markedly prolonged, and she was admitted for observation under telemetry. The following day the patient had experienced a near syncope during an episode of 18 s of Torsade de Pointes (TdP). At the time of TdP, the potassium level (3.4 mmol/L) was mildly reduced, and the ECG showed a QTc interval of 640 ms. In spite of correction of hypokalaemia and discontinuation of the possibly LQTS-inducing drug citalopram the QTc duration remained intermittently prolonged. A transthoracic echocardiogram and a recent coronary angiogram were normal. The patient received an implantable cardioverter-defibrillator. Subsequent genetic testing identified a heterozygous KCNE1 p.D85N (c.253G>A) variant, a known QT modifier with a population prevalence of 1.3%. DISCUSSIONWe conclude that the combination of a commonly prescribed antidepressant, discrete hypokalaemia, and a common KCNE1 QT modifier may cause severe QTc prolongation and life-threatening arrhythmia.